Seasonal Affective Disorders
Said, M, University of Liverpool, UK.
- Diagnostic Assessment
Table 1: SAD criteria of Rosenthal et al (1984)3
|1) A history of major affective disorder, according to Research Diagnostic Criteria (Spitzer et al 1978)4|
|2) At least two consecutive previous years in which the depressions developed during fall or winter and remitted by the following spring or summer|
|3) Absence of any other Axis I DSM-III psychiatric disorder (American Psychiatric Association 1980)|
|4) Absence of any clear-cut seasonally changing psychosocial variables that would account for the seasonal variability in mood and behaviour|
Now the diagnostic term is included in the Diagnostic and Statistical Manual of Mental Disorders (DSM) of the American Psychiatric Association. The DSM-IV is one of two standard diagnostic manuals used by psychiatrists for diagnosis, the other one being the International Classification of Diseases, currently in its 10th edition (World Health Organisation, 1992). The patient must satisfy certain criteria before a diagnosis of SAD can be made (Table 2).
Table 2: DSM-IV criteria for seasonal pattern specifier
Specify if, with seasonal pattern (can be applied to the pattern of major depressive episodes in bipolar I disorder, bipolar II disorder, or major depressive disorder, recurrent):
a. There has been a regular temporal relationship between the onset of major depressive episodes in bipolar I or bipolar II disorder or major depressive disorder, recurrent, and a particular time of year (e.g. regular appearance of the major depressive episode in autumn or winter)
b. Full remissions (or a change from depression to mania or hypomania) also occur at a characteristic time of year (e.g. depression disappears in the spring).
c. In the last 2 years, two major depressive episodes have occurred that demonstrate the temporal season relationship defined in criteria a and b, and no non-seasonal major depressive episode has occurred during the same period.
d. Seasonal major depressive episodes (as described above) substantially outnumber the non-seasonal major depressive episodes that may have occurred over the individual’s lifetime.
Note: Do not include cases in which there is an obvious effect of season-related psychosocial stressors (e.g. regularly being unemployed each winter)
Source: American Psychiatric Association (1994).Typically, winter SAD sufferer would be a patient who has been regularly diagnosed as suffering from major depression during the winter and remits during the summer. Around 30% of patients with SAD also experience a bipolar mood swing from depression to a feeling of elation or ‘high’, usually during spring, which if severe could be diagnosed as a hypomania.
The diagnosis must take into account any psychosocial factors that may be linked to seasonal changes in mood, e.g. unemployment during winter, whereby the effects of the season would not be the causal factor of the mood change. Evidence also shown the existence of a milder form of SAD, ‘subsyndromal SAD’ (S-SAD), which is clinically significant but not severe enough as SAD5.
A study point out that patients are more disturbed by the lethargy and fatigue than by the mood changes themselves, especially in the early phases of their winter depression, therefore often seeking the help of a physician rather than a psychiatrist6. Untreated, SAD episodes generally resolve by springtime, although some do not fully recover before the early summer. Many patients reported that travel to latitudes nearer the equator resulted in remission or diminishing of their symptoms3.
Winter SAD is also seen in children, who present with fatigue, irritability, difficulty getting out of bed in the morning and school problems7. The seasonal pattern of summer is opposite to that of winter SAD with reversal of their winter symptoms in summer.
Table 3 shows the comparison between SAD and non-seasonal depression.
|Sleep||Sleep more/difficulty staying awake. Occasionally, disturbed sleep/early morning wakening||Disturbed sleep/early morning wakening|
|Energy||Fatigue often incapacitating/slump in energy in the afternoon||Tiredness loss of energy|
|Eating||Craving for carbohydrates and sweet foods||Loss of appetite|
|Concentration||Difficult to concentrate often with additional memory impairment||Difficult to concentrate often with additional memory impairment|
|Low mood during the winter, often severe. Remitting in the summer. Some experience short period of hyperactivity (hypomania) in the spring.||Persistent low mood, sometimes labile|
|Sense of misery, loss of self-esteem; sometimes hopelessness and despair. Apathy and flat effect (mood)||Sense of misery, loss of self-esteem; sometimes hopelessness and despair. Apathy and flat effect (mood)|
|Stress and anxiety common||Stress, anxiety and aggitation|
|Less interest in sex||Less interest in sex|
|Irritability, problems relating to people. Withdrawal and isolation||Irritability, problems relating to people. Withdrawal and isolation|
|The atypical symptoms of depression are marked in bold italic and predict a good response to phototherapy in seasonal affective disorder|
Table 3: Symptom comparison5
The prevalence of SAD has been estimated to range from 0 to 9.7% depending on the population that is being sampled5. Women are approximately twice as likely to suffer from SAD than men, which is comparable to gender differences reported in non-seasonal depression although they may reflect bias in sampling10. According to a study, the mean age of onset in SAD appears to be in the thirties11.
Though the geographical distribution of SAD has not been rigorously studied there is evidence to suggest that the prevalence of SAD and S-SAD increases with an increase in northern latitude1. This led to the view that SAD is linked to the hours of daylight that people are exposed to at different latitudes, where the further north a person lives the fewer hours of sunlight exposure per day. Research in different areas of the USA found there was a correlation between latitude and prevalence of SAD (Table 4).
Table 4: The prevalence of SAD and S-SAD in a survey carried out in the USA12
|Location||Latitude (north)||SAD (%)||SAD + S-SAD (%)|
SAD = seasonal affective disorder; S-SAD = subsyndromal SAD.
However, when compared with the results above, several studies have found lower rates of SAD in Iceland and Manitoba which are located at 63-67o north and 50o north respectively13. Even among descendants of Icelandic emigrants in Canada, the prevalence was low suggesting genetic adaptation might play an important role14. This finding seems to emphasize the importance of genetic, psychosocial, cultural and ethnic factors in the development of SAD.
The ‘photon-counting’ hypothesisThe short days of winter deprive susceptible patients of sufficient quanta of light for some chemical process responsible for maintaining a euthymic (normal) state. So this ‘photon deficient’ depression is treated by supplementing the deficient light.
This hypothesis is based on initial report in SAD documenting that bright light acted as an antidepressant whereas dim light did not3 and further supported by data indicating that there is a dose-response relationship for light as well as an inverse relationship between duration and intensity of light required15. A limitation of this hypothesis is that it doesn’t specify what intervening processes are influenced by these varying amounts of lights, which in turn influence the outcome in SAD patients.
The ‘melatonin’ hypothesisThe hormone melatonin plays a role in the secretion and regulation of various hormones and seasonal changes in behaviour. Studies have demonstrated that melatonin is inhibited by bright light and therefore is increased in the darker winter months. So suppression of melatonin by light should induce an antidepressant effect.
The results of several studies have argued against this hypothesis. Firstly, administration of melatonin to successfully treated SAD patients did not induce them to relapse16. Secondly, SAD patients treated with atenolol (beta-adrenergic blocker) that reduces night-time melatonin levels failed to improve their condition17. These and other results suggest that the suppression of pineal melatonin secretion may account for some symptoms that resolve during light therapy, but there is no convincing evidence that it is central to the disorder.
The ‘phase shift’ hypothesisThis concept was built on the capacity of bright light in the evening to delay the nocturnal rise of melatonin and in the morning to advance the rhythm18. So the association between phase-advancing and antidepressant effects of phototherapy suggested a connection between delayed circadian rhythms and depression.
This theory postulates that time of day of phototherapy is critical to the antidepressant response. Few studies rejected this theory because it could be argued that evening light treatment should make patients worse whereas, in fact, the reverse happened19. Nevertheless, circadian rhythms may be linked since the eye may be more sensitive to light in the early morning than at other times. Unanswered questions includes are rhythms really delayed in winter SAD and whether they are the central abnormality.
The ‘amplitude’ hypothesisThis theory was developed from endogenous circadian amplitudes of variables such as temperature, melatonin and heart rate that can be markedly suppressed or enhanced depending upon the timing of light exposure. This suggests that increased circadian amplitude induced by phototherapy may result in the antidepressant effect of light20.
Neurotransmitter hypothesisTwo neurotransmitters may be playing the central roles in the pathophysiology of winter SAD: Dopamine and Serotonin.
Dopamine might play a role in SAD by modulating a ‘behavioural facilitation system’ where evidence of reduced prolactin secretion in SAD patients compared with normal volunteers in both winter and summer suggests that it might be a trait marker of the condition21. This finding might indicate a dopaminergic secretion in SAD, since low basal prolactin secretion may result from compensatory up-regulation of D2-receptors in the anterior pituitary gland associated with low functional activity of dopamine.
Bright light allows dopamine to be produced in the retina and suppresses the production of retinal melatonin thereby improving mood by mechanisms such as resetting the circadian ocular clock or triggering dopaminergic impulses affecting central neuronal structures22.
This neurotransmitter was nominated as one whose functional deficiency might be responsible for depressive disorders in general because the therapeutic effects of some antidepressant drugs may be dependent on serotonin availability23.
Carbohydrate craving may also reflect a functional serotonin deficiency, which would be consistent with the serotonin theory of SAD, given the eminent symptom of carbohydrate cravings in winter depression3.
HormonesWinter SAD patients were shown to have normal basal plasma cortisol and Adrenocorticotrophin Hormone (ACTH) levels, but reduced ACTH responses to infusions of Corticotrophin Hormone that may occur in hypercortisolaemic patients, such as melancholic depressives24.
Other explanation include an underactive Hypothalamus-Pituitary-Adrenal axis associated with the lethargy, hypersomnia and hyperphagia compared to the agitation, insomnia and anorexia seen in melancholic depression.
PhototherapyPhototherapy is a treatment involving daily exposure to high-intensity, broad-spectrum light. The discovery that human melatonin production can be suppressed by bright light led to the initial test of bright light in treating winter depression. The therapeutic effects of phototherapy may involve a serotonergic mechanism since rapid tryptophan (dietary amino acid precursor of serotonin) depletion appears to reverse the antidepressant effect of phototherapy25.
The efficacy of phototherapy has been demonstrated in over 20 placebo-controlled studies around the world26,27. It is difficult to control for the placebo effect in phototherapy studies, since the patients often believe that light will be helpful and the ideal standard of a double-blind design is not possible. Many attempts have been made to control for placebo effects of light by varying intensity, colour and timing of treatment, as well as directing the light to different parts of the body. Several parameters have emerged for optimal use of phototherapy.
Parameters for phototherapy
BrightnessIlluminance, measured in terms of quanta of light sensed over time by a certain surface area or Lux, was the first treatment variable studied systematically. Light boxes delivering 100-850 lux were less effective than brighter units in a series of controlled crossover studies26. Later studies indicated that an overall remission rate of 75% could be achieved using fluorescent light fixtures positioned to produce
10 000 lux28.
TimingSome researches have found that morning is the most effective time for phototherapy, whereas others have found patients to respond well to light at other times of day29. In accordance to the phase-shift hypothesis for winter depression, morning light that causes a circadian phase advance should be more antidepressant than evening light which causes a delay. Since no studies have found that evening light to be more antidepressant than morning light, investigations have shown either no difference30 or morning light to be superior31.
DurationFew studies indicated that the greater the daily duration, the greater the antidepressant effect, however, there is little published evidence that increased antidepressant effects may be achieved using greater than 2-hour light periods/day15.
Duration may also be inversely related to intensity in determining efficacy of treatment32
SpectrumOriginal studies use full-spectrum fluorescent lights, which largely reproduce the distribution and range of visible and ultraviolet light. Recent studies has discussed the comparative merits of different brands of white fluorescent lamp emitting different amounts of ultraviolet radiation but to no avail33 although different wavelengths were demonstrated to have an effect where green light shown to be superior to others. Incandescent light sources may also be effective in the treatment of SAD34.
Route of deliveryLight appears to have its therapeutic effect through the eyes and not the skin in SAD patients35, even though a case report has documented the efficacy of phototherapy in a blind individual36.
When properly administered, phototherapy has no known irreversible side effects. Nevertheless, overexposure to ultraviolet light might adversely affect the eyes or the skin e.g. cortical cataract as a result of excessive long-term exposure to ultraviolet light. Some patients complain of eyestrain, mild headaches, insomnia or hypomanic irritability37.
PharmacotherapyMedications may have a role in the treatment of SAD, even though psychiatrist are aware that it is quite easy to misdiagnose SAD and treatment with conventional antidepressants often exacerbate the atypical symptoms of hypersomnia and carbohydrate craving. There have been few studies to assess how effective antidepressant drugs are in the treatment of SAD, however, the serotonin-agonist d-fenfluramine38 and the Selective Serotonin Reuptake Inhibitor (SSRI) sertraline39 has been found to be a promising treatment. SSRIs are used because of the close association between SAD symptoms and serotonergic neurotransmission. Recently another SSRI, fluoxetine usually used in the treatment of non-seasonal major depression40 also found to be effective after being compared with phototherapy41.
PsychotherapyCognitive behaviour therapy (CBT) helps patients regain a degree of control over their symptoms consequently managing their illness more effectively. Although it may provide some long-term benefit42, CBT alone may not be sufficient to overcome the biological effect experienced by patients in the winter.
Treatment of summer SADPatients with summer depression appear to respond to traditional antidepressant medications but manipulations of the environmental stresses in summer, e.g. heat and humidity, have not yet been demonstrated to be as effective as phototherapy for winter SAD43. It would be more difficult technically to perform controlled studies on the effects of environmental temperature as compared to light.
Summer SAD has been defined but has yet to be fully explored and whether this is a distinct diagnostic syndrome remains debatable. Lastly, more clinical trials on the potential roles of diet and cognitive therapy and the efficacy of various antidepressants in SAD have yet to be undertaken.
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